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Abstract
Glucose is the key source for most organisms to provide energy, as well as the key source for metabolites to generate building blocks in cells. The deregulation of glucose homeostasis occurs in various diseases, including the enhanced aerobic glycolysis that is observed in cancers, and insulin resistance in diabetes. Although p53 is thought to suppress tumorigenesis primarily by inducing cell cycle arrest, apoptosis, and senescence in response to stress, the non-canonical functions of p53 in cellular energy homeostasis and metabolism are also emerging as critical factors for tumor suppression. Increasing evidence suggests that p53 plays a significant role in regulating glucose homeostasis. Furthermore, the p53 family members p63 and p73, as well as gain-of-function p53 mutants, are also involved in glucose metabolism. Indeed, how this protein family regulates cellular energy levels is complicated and difficult to disentangle. This review discusses the roles of the p53 family in multiple metabolic processes, such as glycolysis, gluconeogenesis, aerobic respiration, and autophagy. We also discuss how the dysregulation of the p53 family in these processes leads to diseases such as cancer and diabetes. Elucidating the complexities of the p53 family members in glucose homeostasis will improve our understanding of these diseases. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
Keywords
glucose transporter 3, glucose transporter 4, mitochondrial transcription factor A, monocarboxylate transporter 1, protein p53, protein p63, sirtuin 1, glucose, protein p53, TP63 protein, human, transcription factor, tumor protein p73, tumor suppressor protein, autophagy, dephosphorylation, diabetes mellitus, electron transport, epigenetics, gluconeogenesis, glucose metabolism, glucose transport, glycolysis, human, insulin release, insulin resistance, mitochondrial respiration, nonhuman, oxidative phosphorylation, pentose phosphate cycle, protein expression, Review, transcription regulation, animal, genetics, glycolysis, metabolism, mutation, Animals, Glucose, Glycolysis, Humans, Mutation, Transcription Factors, Tumor Protein p73, Tumor Suppressor Protein p53, Tumor Suppressor Proteins
Source Title
International Journal of Molecular Sciences
Publisher
Series/Report No.
Collections
Rights
Attribution 4.0 International
Date
2018
DOI
10.3390/ijms19030776
Type
Review